Wound healing is an important physiologic process aimed at the restoration of tissue continuity following injury. Activation of the neuroendocrine system by stress has been shown to alter the kinetics of wound healing by increasing serum glucocorticoid levels. This elevation in the level of glucocorticoids is the underlying factor contributing to the impaired healing seen in wounds of restraint stressed animals. Studies suggest that elevated glucocorticoid levels may provoke alterations in the expression of pro-inflammatory cytokines important in the early phases of wound healing. Recent studies suggest that androstenediol (5-androstene-3beta, 17beta-diol, AED) may reduce the immunosuppressive action of glucocorticoids during stress and preferentially augment the production of cytokines necessary for inflammation and resolution of infection. The purpose of this study is to describe how AED will counteract the glucocorticoid-mediated immunosuppressive effects of stress during wound healing. We hypothesize that the health adverse effects of highly elevated GC will be reduced by pharmacological treatment with AED.